Rathert Philipp, Zhang Xing, Freund Christian, Cheng Xiaodong, Jeltsch Albert
Biochemistry Laboratory, School of Engineering and Science, Jacobs University Bremen, Campus Ring 1, 28759 Bremen, Germany.
Chem Biol. 2008 Jan;15(1):5-11. doi: 10.1016/j.chembiol.2007.11.013.
Histone methylation is an epigenetic mark essential for gene regulation and development. We introduce peptide SPOT synthesis to study sequence specificity of the Dim-5 histone-3 lysine-9 methyltransferase. Dim-5 recognizes R8-G12 of the H3 tail with T11 and G12 being the most important specificity determinants. Exchange of H3 tail residue S10 and T11 by E strongly reduced methylation by Dim-5, suggesting that phosphorylation of S10 or T11 may regulate the activity of Dim-5. In the Dim-5/peptide structure, E227 interacts with H3R8 and D209 with H3-S10. Mutations of E227 or D209 caused predictable changes in the substrate preference, illustrating that peptide recognition of histone methyltransferases can be altered by protein design. Comparative analyses of peptide arrays with wild-type and mutant enzymes, therefore, are well suited to investigate the target specificity of protein methyltransferases and study epigenetic crosstalk.
组蛋白甲基化是一种对基因调控和发育至关重要的表观遗传标记。我们引入肽段点合成法来研究二甲基化酶5(Dim-5)组蛋白H3赖氨酸-9甲基转移酶的序列特异性。Dim-5识别H3尾巴的R8-G12区域,其中T11和G12是最重要的特异性决定因素。将H3尾巴残基S10和T11替换为E会显著降低Dim-5的甲基化作用,这表明S10或T11的磷酸化可能调节Dim-5的活性。在Dim-5/肽段结构中,E227与H3R8相互作用,D209与H3-S10相互作用。E227或D209的突变导致底物偏好发生可预测的变化,这说明通过蛋白质设计可以改变组蛋白甲基转移酶的肽段识别。因此,对野生型和突变型酶的肽阵列进行比较分析,非常适合研究蛋白质甲基转移酶的靶标特异性并研究表观遗传串扰。